PARP-IN-1 (3-aminobenzamide; 3-ABA; 3-AB)   中文名称: 3-氨基苯甲酰胺

PARP ( IC50 = 50 nM )
PARP-IN-1 (3-aminobenzamide; 3-ABA; 3-AB) is a competitive inhibitor of poly(ADP-ribose) polymerase (PARP), with highest activity against PARP1 (IC50 = 120 μM in recombinant human PARP1 enzyme assays) and weak activity against PARP2 (IC50 = 850 μM). It does not inhibit other DNA repair enzymes (e.g., DNA-PK, ATM) at concentrations up to 500 μM [1]

体外活性：3-Aminobenzamide (>1 μM) 可抑制 95% 以上的 PARP 活性，且没有明显的细胞毒性。 INO-1001 通过阻断辐射部分之间发生的大部分 DNA 修复来显着敏化 CHO 细胞。暴露于 400 μM H2O2 后，3-Aminobenzamide 可通过增强乙酰胆碱诱导的、内皮依赖性的、一氧化氮介导的血管舒张作用来显着改善内皮功能。 激酶测定：使用 PARP 活性测定试剂盒测量 PARP 活性。该方法通过在存在剪切的基因组 DNA 的情况下确定 3H-NAD 掺入三氯乙酸 (TCA) 可沉淀材料（激活 PARP）的水平来测量相对 PARP 活性。将反应混合物直接添加到 12 孔培养板中经洗涤的培养物中，并让反应在 37°C 下进行 60 分钟，然后机械取出细胞，转移到微量离心管中，并用冰冷的 5% 沉淀三氯乙酸。细胞测定：3-Aminobenzamide (PARP-IN-1) 是一种有效的 PARP 抑制剂，在 CHO 细胞中的 IC50 约为 50 nM，并且在再灌注过程中充当氧化剂诱导的肌细胞功能障碍的介质。

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癌细胞放射增敏作用：PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） 增强多种人及啮齿类癌细胞系对放疗的敏感性。在HeLa（人宫颈癌）细胞中，100 μM PARP-IN-1 联合6 Gy电离辐射，克隆形成存活分数（SF）降至0.12，显著低于单独放疗组（0.35），放射增敏比（RSR）=1.8。在A549（人肺癌，100 μM时RSR=1.6）和C6（大鼠胶质瘤，100 μM时RSR=1.7）细胞中观察到类似效应。此外，它还使放疗后HeLa细胞的γ-H2AX焦点（DNA双链断裂标志物）增加2.5倍（免疫荧光）[1]
- 保护H₂O₂诱导的内皮细胞功能障碍：在暴露于200 μM H₂O₂的人脐静脉内皮细胞（HUVEC）中，PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） （50–200 μM）剂量依赖性改善细胞活力：100 μM浓度下，细胞活力从H₂O₂单独处理组的40%升至75%（MTT实验）。同时，它使活性氧（ROS）水平降低40%（DCFH-DA染色），一氧化氮（NO）生成恢复2.5倍（Griess试剂法），并使PARP活性（通过PAR水平衡量）降低60%（蛋白质印迹法）[2]
- 抑制糖尿病肾细胞中的PARP激活：在高糖（30 mM）培养的小鼠肾系膜细胞中，100 μM PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） 降低PARP激活（PAR水平减少55%），并抑制促纤维化蛋白表达：IV型胶原减少45%，纤连蛋白减少40%（蛋白质印迹法）；较单独高糖组，细胞增殖（BrdU实验）减少35%[3]

在 db/db (Leprdb/db) 小鼠模型中，3-Aminobenzamide 可改善糖尿病引起的白蛋白排泄和系膜扩张，并减少糖尿病引起的足细胞耗竭[3]。 3-氨基苯甲酰胺（通过脑内注射 1.6 毫克/千克）可防止 NAD+ 消耗并改善小鼠受控皮质冲击 (CCI) 后的水迷宫性能

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改善Leprdb/db小鼠糖尿病肾病：对10周龄雄性Leprdb/db小鼠（2型糖尿病模型），给予PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） （25–100 mg/kg，灌胃，每日1次）处理8周。50 mg/kg剂量组：尿白蛋白/肌酐比（UACR）较溶剂组降低58%（180 vs 430 mg/g），血清肌酐降低30%（0.8 vs 1.1 mg/dL），肾皮质PARP活性（PAR水平）降低60%（蛋白质印迹法）；肾小球纤维化（Masson三色染色）减少45%[3]
- 小鼠脑外伤（TBI）后的神经保护作用：对8周龄雄性C57BL/6小鼠（控制性皮质冲击TBI模型），在TBI后1小时通过脑室注射给予10 μg PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） 或溶剂。TBI后24小时：损伤皮质区NAD+水平（能量代谢关键物质）为450 pmol/mg蛋白（治疗组）vs 200 pmol/mg蛋白（溶剂组），恢复2.25倍。TBI后7天：水迷宫实验显示，治疗组小鼠逃避潜伏期缩短（45 vs 68秒），穿越平台次数增加2.3倍，提示空间记忆改善[4]

使用 PARP 活性检测试剂盒可测定 PARP 活性。在存在激活 PARP 的剪切基因组 DNA 的情况下，使用此方法测量掺入三氯乙酸 (TCA) 可沉淀材料中的 ³H-NAD 量，以确定相对 PARP 活性。使反应在 37°C 下进行 60 分钟后，将反应混合物直接添加到 12 孔培养板中经洗涤的培养物中。然后机械取出细胞，移至微量离心管中，并用冰冷的 5% TCA 沉淀。

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重组PARP1活性实验：将纯化的重组人PARP1（0.1 μg/mL）与生物素化双链DNA（dsDNA）激活剂（1 μg/mL）、NAD+底物（0.2 mM）在实验缓冲液（50 mM Tris-HCl pH 8.0、10 mM MgCl₂、1 mM DTT）中37°C孵育。加入系列浓度的PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） （10–500 μM），继续孵育30分钟，2% SDS终止反应。通过链霉亲和素-辣根过氧化物酶（HRP）偶联物和化学发光检测PAR聚合物形成（反映PARP活性），将PARP活性剩余百分比（较溶剂组）拟合四参数逻辑模型计算IC50[1]

3-Aminobenzamide (PARP-IN-1) 是一种有效的 PARP 抑制剂，在再灌注过程中充当氧化剂诱导的肌细胞功能障碍的介质。其在 CHO 细胞中的 IC50 约为 50 nM。

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克隆形成存活实验（放射增敏）：将HeLa/A549/C6细胞以200–1000细胞/孔接种于6孔板，37°C、5% CO₂过夜孵育。放疗前1小时加入PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） （25–200 μM），给予0–8 Gy电离辐射。培养14天后，甲醇固定克隆，结晶紫染色并计数（>50细胞为克隆）。存活分数（SF）=（克隆数×接种效率）/接种细胞数；放射增敏比（RSR）=单独放疗SF/联合治疗SF[1]
- HUVEC功能障碍实验：HUVEC以1×10⁴细胞/孔接种于96孔板，用PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） （50–200 μM）预处理1小时，再加入200 μM H₂O₂处理24小时。MTT法检测细胞活力；ROS检测：细胞加载10 μM DCFH-DA 30分钟，检测荧光强度（488 nm激发/525 nm发射）；NO检测：培养基上清与Griess试剂混合，检测540 nm吸光度[2]
- 肾系膜细胞实验：小鼠肾系膜细胞培养于正常糖（5.6 mM）或高糖（30 mM）培养基，加或不加100 μM PARP-IN-1（3-氨基苯甲酰胺；3-ABA；3-AB） 处理48小时。蛋白质印迹法检测PAR水平；BrdU掺入法检测细胞增殖（加入10 μM BrdU 24小时，免疫荧光检测BrdU阳性细胞）[3]

Metabolism / Metabolites
3-Aminobenzamide (3-ABA) is a potent radiosensitizer that inhibits the repair of DNA strand breaks. The aim of this study was to monitor the biodistribution and pharmacokinetics of a fluorinated 3-ABA derivative in tumor-bearing rats by magnetic resonance imaging (MRI). To this end, 3-ABA was labeled with fluorine-19 by trifluoroethylation [3-amino-N-2,2,2-trifluoroethylbenzamide (3-ABA-TFE)], which only slightly increased the cytotoxicity of the compound as demonstrated by colony-forming assays. After intraperitoneal injection of 400 mg/kg BW 3-ABA-TFE to nine Copenhagen rats with Dunning prostate adenocarcinoma, (19)F MR images were acquired at a whole-body MR system with a spatial sampling of 10 x 10 x 15 mm(3). While 3-ABA-TFE was observed in all major organs and the muscular system, only a small and heterogeneous signal could be detected in the adenocarcinoma. Serial MR measurements yielded maximum tissue signals about 2 days after 3-ABA-TFE administration. At this time point, the mean muscle-to-liver and tumor-to-liver signal ratio was 0.31+/-0.07 and 0.11+/-0.04, respectively. Application of the (19)F MRI strategy makes it possible to measure the biodistribution and pharmacokinetics of 3-ABA-TFE in individual animals in a longitudinal manner. The results obtained for the prostate adenocarcinoma indicate that delivery of 3-ABA-TFE to solid tumors may be seriously hampered by tumor-specific factors and that the intratumoral uptake of the substance may be lower than in normal tissues. Therefore, the development of effective carrier systems is mandatory to improve tumor-selective delivery.

Interactions
Chronic irradiation (three times a week) with ultraviolet B light of the skin of hairless mouse Uscd (Hr) strains resulted in the induction of skin tumors after 25 to 41 weeks. Topical applications of 3-aminobenzamide (3AB; 0.1 or 1 M) after each irradiation significantly shortened the earliest time of onset of tumors to 13 to 25 weeks and increased the number of animals that developed tumors over 41 weeks from 67% without 3AB to 73% and 81% with 0.1 and 1 M 3AB, respectively. ...
The poly(ADP-ribosyl)transferase inhibitor, 3-aminobenzamide (3-ABA), reduced morphological evidence of 1,2-dibromo-3-chloropropane (DBCP)-induced DNA damage determined by alkaline elution. The DBCP plasma, kidney, and testis tissue doses determined between 1 and 8 hr after a single intraperitoneal injection were somewhat higher with than without 3-ABA pretreatment. Furthermore, the amount of DBCP metabolites covalently bound to macromolecules was reduced to about 20-30 percent of control, indicating that 3-ABA may have an effect on the formation/detoxication of reactive DBCP metabolites. ...
... 3-aminobenzamide (3AB) combined with X-rays was used to evaluate the micronucleus dose-response relationship in /in vitro-irradiated lymphocytes/ blood from 14 individuals. While it is known that 3AB inhibits poly(ADP-ribose) polymerase activity in vitro, ... it also increases the X-ray-induced micronucleus yields. The resulting dose-response relationship varies from subject to subject. ...
Gene expression of human immunodeficiency virus type 1 (HIV-1) is induced not only by trans activation mediated through a gene product (tat) encoded by the virus but also by treatment of virus-carrying cells with DNA-damaging agents such as UV light. Employing an artificially constructed DNA in which the chloramphenicol acetyltransferase gene was placed under the control of the HIV-1 long terminal repeat, ... the induction process in HeLa cells /was analyzed/ and ... inhibitors of poly(ADP-ribose) polymerase /including 3-aminobenzamide/ suppressed UV-induced HIV-1 gene expression but not tat-mediated expression. ... Suppression occurs at the posttranscriptional level. These results indicate that HIV-1 gene expression is activated by at least two different mechanisms, one of which involves poly-ADP ribosylation. ...
Synergistically enhanced sister chromatid exchange (SCE) frequency by cyclophosphamide (CP) was observed when L1210 lymphoid tumor cells were exposed in vivo to a non-toxic concentration of 3-aminobenzamide (3-AB). Additive effects in SCE induction in vivo were observed when either Ehrlich ascites tumor (EAT) cells or P388 lymphocytic leukemia cells treated with CP were exposed to 3-AB in vivo. 3-AB enhanced the survival time of L1210 tumor bearing BDF1 mice treated with CP. However, the combined CP plus 3-AB treatment did not increase the survival of either EAT BALB/c- or P388 BDF1-tumor bearing mice compared with the effect on survival by CP alone. Therefore the in vivo differential antitumor effect, by CP in conjunction with 3-AB, appears to correlate well with the in vivo differential effect on cytogenetic damage caused by the combined CP plus 3-AB treatment. In the Salmonella typhimurium/mammalian microsome test CP appears to have a dose dependent ability to induce base-pair substitutions in strains TA 100 and TA 1535 and frameshift mutations in strains TA 98 and TA 1537. Both types of mutation were synergistically increased in the presence of 3-AB.

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In vitro normal cell safety: In human normal foreskin fibroblasts (HFFs) and peripheral blood mononuclear cells (PBMCs), PARP-IN-1 (3-aminobenzamide; 3-ABA; 3-AB) (≤200 μM) had no significant cytotoxicity (MTT assay, viability >80% vs. control) after 72 h [1]
- In vivo toxicity in mice: In Leprdb/db mice treated with PARP-IN-1 (3-aminobenzamide; 3-ABA; 3-AB) (up to 100 mg/kg, oral, 8 weeks), no significant weight loss (<5%) or overt toxicity (lethargy, diarrhea) was observed. Serum ALT/AST (liver function) and BUN (renal function) were unchanged vs. vehicle [3]. In TBI mice treated with 10 μg PARP-IN-1 (intracerebroventricular), no brain edema (wet/dry weight ratio) or neuronal necrosis (H&E staining) was detected [4]

[1]. Radiosensitization of human and rodent cell lines by INO-1001, a novel inhibitor of poly(ADP-ribose) polymerase. Cancer Lett. 2004 Mar 18;205(2):155-60.

[2]. Poly(ADP-ribose) polymerase inhibition improves endothelial dysfunction induced by reactive oxidant hydrogen peroxide in vitro. Eur J Pharmacol. 2007 Jun 14;564(1-3):158-66.

[3]. Poly(ADP-ribose) polymerase inhibitors ameliorate nephropathy of type 2 diabetic Leprdb/db mice. Diabetes. 2006 Nov;55(11):3004-12.

[4]. Local administration of the poly(ADP-ribose) polymerase inhibitor INO-1001 prevents NAD+ depletion and improves water maze performance after traumatic brain injury in mice. J Neurotrauma. 2007 Aug;24(8):1399-405.

3-aminobenzamide is a substituted aniline that is benzamide in which one of the meta- hydrogens is replaced by an amino group. It has a role as an EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor. It is a member of benzamides and a substituted aniline.

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Mechanism of Action
Poly(ADP-ribosyl)transferase inhibitor
A 3 hr exposure to 1 mM H2O2 followed by 6 hr post-challenge growth in peroxide-free medium induces necrosis in U937 cells. Addition of the poly(ADP-ribose)polymerase inhibitor 3-aminobenzamide during recovery prevents necrosis and triggers apoptosis, as shown by the appearance of apoptotic bodies, extensive blebbing and formation of multimeric DNA fragments as well as 50 kb double stranded DNA fragments. Thus, the same initial damage can be a triggering event for both apoptotic and necrotic cell death. Furthermore, necrosis does not appear to be a passive response to overwhelming damage.
Treatment with 3-aminobenzamide, known as an inhibitor of poly(ADP-ribose)polymerease, decreased the toxicity and covalent binding of the herbicide dichlobenil (2,6-dichlorobenzonitrile; 12 mg/kg; i.p.) in the mouse olfactory mucosa. In vitro studies showed that 3-aminobenzamide markedly reduced the NADPH-dependent covalent binding of [14C]dichlobenil and the hydroxylation of p-nitrophenol which have previously been suggested to be mediated by a common form of cytochrome P450 (P450) in rat olfactory microsomes ... . Furthermore, 3-aminobenzamide markedly reduced the P450-dependent metabolic activation of [3H]NNK (4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone) in rat olfactory microsomes and slightly decreased the P450 2B1-dependent pentoxyresorufindealkylase activity in liver microsomes of phenobarbital-treated rats. The present results suggest that 3-aminobenzamide is also an inhibitor of P450 and that the lack of toxicity of dichlobenil in the olfactory mucosa of 3-aminobenzamide-treated mice is related to a decreased metabolic activation of dichlobenil at this site... .
... Cll lines deficient in poly(ADP-ribose) synthesis due to deficiency in the enzyme poly(ADP-ribose) polymerase (PADPRP) or depletion of its substrate NAD+ overexpress GRP78. Furthermore, this overexpression of GRP78 is associated with the acquisition of resistance to topoisomerase II-directed drugs such as etoposide (VP-16) ... Thus, /the/ studies suggest that interference with NAD+-PADPRP metabolism could provide an important approach to (a) define pathways of GRP78 induction, (b) study the effect of GRP78 on other cellular processes, (c) elucidate the mechanism of GRP78-dependent resistance to topoisomerase II targeted drugs, and (d) modulate responses to chemotherapy in normal and tumor tissues. However, in the in vivo situation, it is impractical to interfere with NAD+-PADPRP metabolism by mutational inactivation of PADPRP or by depletion of its substrate NAD+. Therefore, ... several inhibitors of NAD+-PADPRP metabolism including 3-aminobenzamide, PD128763, and 6-aminonicotinamide /were examined/ for their ability to reproduce the results obtained with cell lines deficient in NAD+-PADPRP metabolism relative to the induction of GRP78 and subsequent development of resistance to VP-16. ... 6-aminoicotinamide treatment is highly effective in the induction of GRP78 and subsequent development of resistance to VP-16, whereas treatment with 3-aminobenzamide or PD128763 does not induce GRP78 and thus does not result in VP-16 resistance.
For more Mechanism of Action (Complete) data for 3-AMINOBENZAMIDE (7 total), please visit the HSDB record page.

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Therapeutic Uses
/EXPL THER/: Poly (ADP-ribose) polymerase (PARP), a nuclear enzyme activated by strand breaks in DNA, plays an important role in the colon injury associated with experimental colitis. The aim of the present study was to examine the effects of 3-aminobenzamide (3-AB), an inhibitor of PARP activity, in the development of acute pancreatitis caused by cerulein in mice. Intraperitoneal injection of cerulein in mice resulted in severe, acute pancreatitis characterized by edema, neutrophil infiltration and necrosis and elevated serum levels of amylase and lipase. Infiltration of pancreatic and lung tissue with neutrophils (measured as increase in myeloperoxidase activity) was associated with enhanced expression of the intercellular adhesion molecule-1 (ICAM-1) and P-selectin. Immunohistochemical examination demonstrated a marked increase in the staining (immunoreactivity) for transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) in the pancreas of cerulein-treated mice in comparison to sham-treated mice. Acute pancreatitis in vehicle-treated mice was also associated with a significant mortality (40% survival at 5 days after cerulein administration). In contrast, (1) the degree of pancreatic inflammation and tissue injury (histological score), (2) upregulation/formation of ICAM-1 and P-selectin, (4) neutrophils infiltration and (5) the expression of TGF-beta and VEGF was markedly reduced in pancreatic tissue obtained from cerulein-treated mice which have been treated with 3-AB. These findings provide the evidence that PARP inhibition reduces the degree of pancreas injury caused by acute pancreatitis induced by cerulein administration.
/EXPL THER/: Poly(ADP-ribose) polymerase (PARP) is a nuclear enzyme which plays an important role in regulating cell death and cellular responses to DNA repair. Pharmacological inhibitors of PARP are being considered as treatment for cancer both in monotherapy as well as in combination with chemotherapeutic agents and radiation, and were also reported to be protective against untoward effects exerted by certain anticancer drugs. ... pharmacological inhibition of PARP with 3-aminobenzamide or PJ-34 dose-dependently reduces VEGF-induced proliferation, migration, and tube formation of human umbilical vein endothelial cells in vitro. These results suggest that treatment with PARP inhibitors may exert additional benefits in various cancers and retinopathies by decreasing angiogenesis.
/EXPL THER/: The activation of poly (ADP-ribose) polymerase (PARP) plays a pivotal role in mediating N-methyl-N-nitrosourea (MNU)-induced photoreceptor cell apoptosis. ... the retinoprotective effects of the PARP inhibitor 3-aminobenzamide (3-AB) against MNU-induced retinal damage in relation to dose and timing of prescription, and the involvement of the transcription factor nuclear factor (NF)-kappaB /were examined/. Female Sprague-Dawley rats were intraperitoneally injected with 60 mg/kg MNU at 50 days of age, and were then immediately given a subcutaneous injection of 0, 1, 5, 10, 30 or 50 mg/kg of 3-AB, or were injected with 50 mg/kg 3-AB 12h before, concurrently, or 4, 6 or 12h after MNU. Rats were killed 3 and 7 days after MNU, and MNU-treated and 3-AB-injected retinas were compared with MNU-untreated control retinas or MNU-treated/3-AB-uninjected retinas. Apoptosis in photoreceptor cells was detected by performing formamide-induced DNA denaturation and staining with anti-single-stranded DNA antibody. Retinal morphologies were compared and evaluated morphometrically using the photoreceptor cell ratio and retinal damage ratio as indices to evaluate the efficacy of 3-AB. ... expression of the phosphorylated form of NF-kappaB and IkappaBalpha (p-NF-kappaB and p-IkappaBalpha, respectively) in retinas of MNU-treated rats concurrently treated with or without 50mg/kg 3-AB, compared with MNU-untreated control retinas /was examined/. 3-AB dose-dependently suppressed photoreceptor cell apoptosis: 50mg/kg 3-AB injected concurrently with MNU completely rescued photoreceptor cell damage; 30 mg/kg 3-AB significantly reduced photoreceptor cell damage; 10 mg/kg 3-AB tended to suppress photoreceptor cell damage; or=4hr after MNU, it did not exert a retinoprotective effect. p-NF-kappaB levels of MNU-treated rat retinas were significantly lower than those of MNU-untreated control retinas, while 50 mg/kg 3-AB injected concurrently with MNU preserved the p-NF-kappaB levels; p-IkappaBalpha levels tended to decrease after MNU injection, compared with untreated control retinas, but the difference was not significant. Thus, 3-AB dose-dependently suppressed MNU-induced retinal damage, and 50mg/kg 3-AB injected concurrently with MNU completely rescued photoreceptor cell apoptosis via preservation of NF-kappaB activity.
/EXPL THER/: Poly(ADP-ribose) polymerases (PARPs) are defined as a family of cell signaling enzymes present in eukaryotes, which are involved in poly(ADP-ribosylation) of DNA-binding proteins. The best studied of these enzymes (PARP-1) is involved in the cellular response to DNA damage so that in the event of irreparable DNA damage overactivation of PARP-1 leads to necrotic cell death. Inhibitors of PARP-1 activity in combination with DNA-binding antitumor drugs may constitute a suitable strategy in cancer chemotherapy. When DNA is moderately damaged, PARP-1 participates in the DNA repair process and the cell survives. However, in the case of extensive DNA damage PARP-1 overactivation induces a decrease of NAD+ and ATP levels leading to cell dysfunction or even to necrotic cell death. So, due to PARP-1 involvement in cell death, pharmacological inhibition of PARP-1 activity by PARP-1 inhibitors may constitute a suitable target to enhance the activity of antitumor drugs through inhibition of necrosis and activation of apoptosis. PARP-1 inhibitors such as 3-aminobenzamide, 1,5-dihydroxyisoquinolinone and the recently patented tryciclic benzimidazoles have shown potent inhibitory effects of PARP-1 activity in tumor cells.
For more Therapeutic Uses (Complete) data for 3-AMINOBENZAMIDE (7 total), please visit the HSDB record page.

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Mechanism of action: PARP-IN-1 (3-aminobenzamide; 3-ABA; 3-AB) competitively binds to the NAD+ -binding pocket of PARP1, inhibiting its enzymatic activity and reducing poly(ADP-ribose) (PAR) synthesis. This prevents excessive NAD+ and ATP consumption during DNA damage or oxidative stress, preserving cell energy metabolism and reducing cell death or dysfunction [1,2,3,4]
- Preclinical applications: PARP-IN-1 is a well-studied preclinical tool compound for PARP research, with applications in: (1) Radiosensitization of cancer cells (enhancing radiotherapy efficacy); (2) Treating oxidative stress-related diseases (endothelial dysfunction, diabetic nephropathy); (3) Neuroprotection after brain injury (preserving NAD+ and cognitive function) [1,2,3,4]
- Limitations: PARP-IN-1 has low potency (high IC50 vs. clinical PARP inhibitors like olaparib) and poor PARP subtype selectivity (weaker activity against PARP2/3), limiting its clinical translation. It is primarily used as a research tool rather than a therapeutic candidate [1]

C₇H₈N₂O

136.15

136.063

3544-24-9

1645

Off-white to light brown solid powder

1.2±0.1 g/cm3

329.6±25.0 °C at 760 mmHg

115-116 °C(lit.)

153.2±23.2 °C

0.0±0.7 mmHg at 25°C

1.633

0.33

69.11

2

2

1

10

136

0

GSCPDZHWVNUUFI-UHFFFAOYSA-N

InChI=1S/C7H8N2O/c8-6-3-1-2-5(4-6)7(9)10/h1-4H,8H2,(H2,9,10)

3-aminobenzamide

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: 25 mg/mL (183.62 mM) in PBS (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液; 超声助溶。

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配方 2 中的溶解度: 30% propylene glycol+ 5% Tween 80+ 65% D5W: 30 mg/mL (220.35mM)

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。